Psychosocial Stressors at Work and Atrial Fibrillation Incidence: An 18‐Year Prospective Study
Journal of the American Heart Association
Abstract
Background
Psychosocial stressors at work, defined by the job strain and effort–reward imbalance at work (ERI) models, were shown to increase coronary heart disease risk. No previous study has examined the adverse effect of psychosocial stressors at work from both models on atrial fibrillation (AF) incidence. The objective of this study was to examine the separate and combined effect of psychosocial stressors at work from the job strain and ERI models on AF incidence in a prospective cohort study.
Methods and Results
A total of 5926 white‐collar workers (3021 women and 2905 men) free of cardiovascular disease at baseline were followed for an average of 18 years. Job strain (high psychological demands combined with low decision latitude) and ERI were assessed using validated instruments. AF events were identified in medical databases with universal coverage. Hazard ratios (HRs) with 95% CIs were estimated using Cox regression models, controlling for socioeconomic characteristics and lifestyle‐related and clinical risk factors. A total of 186 AF incident events were identified over 18 years. Workers exposed to job strain (HR, 1.83 [95% CI, 1.14–2.92]) and ERI (HR, 1.44 [95% CI, 1.05–1.98]) had a higher risk of AF in fully adjusted models. Combined exposure to job strain and ERI was associated with a 2‐fold AF risk increase (HR, 1.97 [95% CI, 1.26–3.07]).
Conclusions
Psychosocial stressors at work from the job strain and ERI models are associated with an increased risk of AF, separately and in combination. Workplace prevention strategies targeting these psychosocial stressors at work may be effective to reduce the burden associated with AF.
Nonstandard Abbreviations and Acronyms
- ERI
- effort–reward imbalance
- PROQ
- Prospective Quebec Study on Work and Health
Clinical Perspective
What Is New?
•
In this prospective cohort study, workers exposed to psychosocial stressors at work from the job strain and effort–reward imbalance models had an increased risk of atrial fibrillation.
What Are the Clinical Implications?
•
Reducing psychosocial stressors at work may be an effective strategy to improve the prevention of atrial fibrillation.
•
Clinical awareness on these work stressors and their adverse effect on cardiovascular health is needed.
Atrial fibrillation (AF) is the most common form of arrythmia, affecting about 1 in 4 men and women aged >40 years in their lifetime.1 AF increases the risk of strokes, heart failure, and other cardiovascular complications.2 Individuals with AF have higher morbidity, as measured with disability‐adjusted life years.3 With the worldwide aging of the population, it is estimated that from 2010 to 2060, the number of adults aged ≥55 years with AF will more than double.4 To address the increasing public health and economic burden associated with AF, primary prevention is critical.5 Modifiable lifestyle‐related risk factors including alcohol intake and cigarette smoking have been identified as AF risk factors.6, 7
Psychosocial stressors at work are modifiable risk factors from the work environment that were shown to increase coronary heart disease (CHD) risk.8 Two main models have been used to assess the adverse effect of psychosocial stressors at work. The demand–control model (ie, job strain) suggests that workers simultaneously experiencing high psychological demands and low decision latitude are more likely to develop stress‐related health problems.9 Siegrist's effort–reward imbalance model (ERI) suggests that efforts should be rewarded in various ways: income, respect and esteem, and occupational status control. Workers are in a state of harmful imbalance when high efforts come with low reward and thus more susceptible to health problems.10 Psychosocial stressors at work from the job strain and ERI models are complementary both theoretically and empirically.11 Theoretically, job strain refers to the quantity and characteristics of work tasks. It acts as a threat to our need for autonomy, triggering an adverse stress response mechanism. The ERI model relies on the concept of social reciprocity, a central concept of the employment contract in which social actors expect to receive rewards in exchange for efforts invested at work.12, 13 Empirically, previous studies have documented the effect of psychosocial stressors at work from both models on the risk of CHDs.8
However, few prospective studies have assessed the effect of psychosocial stressors at work on AF incidence. Available evidence suggests that psychosocial stressors at work from the job strain model is associated with an increased risk of AF.14, 15, 16 There is no evidence about the effect of ERI, and the effect of combined exposure remains unknown. The aim of the present study was to examine the separate and combined effect of psychosocial stressors at work from the job strain and ERI models on AF incidence in an 18‐year prospective study of men and women without cardiovascular disease (CVD) at entry.
METHODS
Study Design and Population
The PROQ (Prospective Quebec Study on Work and Health) was initiated in the Quebec region in 1991 to 1993. Details have been published elsewhere.17 Figure 1 presents the study flowchart. In brief, 9188 white‐collar workers from 19 public and semipublic organizations were recruited (1991–1993, T1). The participation rate was 75%. At the first follow‐up 8 years later (1999–2001, T2), 8046 subjects participated and were linked with medical databases (87.6%). The current study baseline was set at T2 since ERI was first assessed at that time. Participants were initially screened based on inclusion criteria. Those with a prior AF event (n=41) or CVD event (n=343) before T2 were not eligible. Furthermore, retired and inactive participants at T2 (n=1001) did not meet the inclusion criteria. Participants with missing data on exposures or covariates were excluded (n=735). The final sample consisted of 5926 workers.
Figure 1. Study flowchart.
*75% participation rate at recruitment. †Participants missing the necessary information to be recontacted at follow‐up. ‡8046/9188 (87.6%)=participation rate at T2; §Do not have job according to self‐reported questionnaire at T2. AF indicates atrial fibrillation; CVD, cardiovascular disease; PROQ, Prospective Quebec Study on Work and Health; and RAMQ, Régie de l'Assurance Maladie du Québec (Quebec Health Insurance Board).
The present study was approved by the ethics review board of Centre Hospitalier Universitaire (Hospital Research Center) de Quebec‐ Université Laval. All patients provided informed consent. The data that support the findings of this study are available from the corresponding author on reasonable request ([email protected]).
Psychosocial Stressors at Work
Psychosocial stressors at work were measured using validated instruments according to the job strain9 and ERI models.10
Job Strain
Psychological demands and decision latitude were measured using the 18 items from Karasek's Job Content Questionnaire. The psychometric properties of the original scale18, 19 and its French version19, 20, 21, 22 have been demonstrated. Psychological demands refer to an excessive workload, task interruption, intense concentration, and conflicting demands. Decision latitude refers to skill discretion and decision autonomy. Responses were compiled with a 4‐point Likert‐type scale and summed to obtain a total score for psychological demands (range, 9–36) and decision latitude (range, 24–96). The median for the general Quebec working population was used to classify workers as having high psychological demand (≥24) and low decision latitude (≤72).23 Accordingly, the recommended quadrant method was used to classify workers into 4 groups: those with low job strain (low psychological demand, high decision latitude; reference category); passive jobs (low psychological demand, low decision latitude); active jobs (high psychological demand, high decision latitude); and those experiencing high job strain (high psychological demand, low decision latitude).
ERI at Work
Reward at work was measured by 9 original questions from the French version10, 24, 25 of the ERI scale (3 of 5 questions from the esteem subscale, the 4‐item subscale of promotion prospects and salary, and the 2‐item subscale of job security). The questions were answered in 2 steps.25 The respondents were first asked to indicate whether they agreed or disagreed that the question content described an experience typical of their work situation. If they agreed, they were then asked to indicate to what extent they felt distressed by the experience, with 1=very distressed, 2=distressed, 3=somewhat distressed, and 4=not at all distressed (scores were inverted for positive items).
Effort was measured by 9 items from the validated French version of the psychological demand scale of the Job Content Questionnaire.21, 26 Effort and reward score range was unified (range, 9–27). The psychometric qualities of this ERI version have been demonstrated.27 ERI ratio was computed using effort as the numerator and reward as the denominator. ERI ratio was analyzed as a dichotomous variable, with a high‐risk exposure defined as an ERI ratio of >1.
Combined Exposure
Combined exposure to both job strain and ERI was defined as follows: “Double exposure” refers to participants exposed simultaneously to psychosocial stressors at work from the job strain and ERI models. “Intermediate” exposure refers to participants exposed to either job strain or ERI, but not both. The reference category comprised the remaining participants (exposed to neither work stressor).
Atrial Fibrillation
AF events were identified in medical databases including all hospitalizations, emergency visits, and outpatient consultations, within the context of the universal health care coverage in the province of Quebec.28 AF diagnostic codes were identified using the International Classification of Diseases, Ninth Revision (ICD‐9; 427.3, 427.31) and Tenth Revision (ICD‐10, Canadian version; I48.0, I48.00, I48.01, I48.02, I48.90).29 A validated definition was used (sensitivity, 70.8%; specificity, 99.2%; positive predictive value, 70.8%, using electronic medical records as the gold standard).29 Participants were identified with an incident AF event if they had (1) at least 1 hospitalization with a diagnosis of AF, (2) at least 1 emergency room record, or (3) ≥4 physician consultations in 1 year with a 30‐day separation between consultations. The date of AF was defined as the date of the first occurrence of 1 of these conditions. CHD and heart failure events were identified using the same method. Details are provided in Data S1.
Covariates
The following covariates were considered as potential confounders. Sociodemographic characteristics were age, sex, and education. Lifestyle‐related risk factors including cigarette smoking, alcohol consumption, and physical activity were assessed. Smoking status was defined using 3 categories (never smoker, former smoker, and current smoker).30 Alcohol consumption was categorized into 3 groups using the guidelines of the time, on the basis of the weekly frequency of intake: low consumption (<1 drink per week), moderate consumption (1–10 drinks per week for women and 1–15 for men), and high consumption (>10 drinks per week for women and >15 for men).31 A validated measure of leisure‐time physical activity based on frequency and duration was used.32 The 3‐level categorization was low level of physical activity (<1 leisure physical activity of 20–30 minutes weekly); moderately active (1 or 2 leisure physical activities); and active (≥3 leisure physical activities). Diabetes, hypercholesterolemia, antihypertensive medication, and family history of CVD were assessed with a self‐reported questionnaire. Weight and height were measured by a trained research nurse according to a validated protocol. Body mass index was calculated as the ratio between weight in kilograms and the square of height in meters. Resting blood pressure (BP) was measured by a trained nurse according to a validated protocol.33 Participants were identified with hypertension if the average of two BP measurements were elevated (systolic BP ≥140 mm Hg or diastolic BP ≥90 mm Hg).
Statistical Analysis
Cox proportional hazards models, with age as the time scale, were used to estimate hazard ratios (HRs) and their 95% CIs. By using age as the time scale and allowing for delayed entry at baseline age, the hazard was modeled as a function of the individuals' changing age, rather than the arbitrary time elapsed since the beginning of follow‐up. The proportional hazards assumption of the Cox model was visually verified using Schoenfeld residuals and was deemed satisfied. Follow‐up time was measured from the study baseline (T2, 1999–2001) until the first occurrence of AF, death, loss to follow‐up (ie, moving outside of the Quebec province; n=4) or the end of the study (December 31, 2018), whichever came first. As recommended for etiologic studies, follow‐up times were right censored at the time of competing risks (ie, death).34 The multivariable analyses were sequentially adjusted for each group of covariables to examine the potential overadjustment by mediating factors (Figure S1). Models were sequentially adjusted for (1) age (time scale); (2) socioeconomic characteristics (sex and education); (3) lifestyle‐related risk factors (smoking, alcohol, and physical activity), and (4) clinical risk factors (diabetes, hypertension, antihypertensive medication, hypercholesterolemia, and family history of CVD and body mass index). Cumulative incidence curves with age as the time scale were obtained from the survival functions in a Cox regression model.
Sensitivity analyses were conducted. AF events occurring within the first 5 years of follow‐up were excluded, to consider a potential induction period. Censoring at retirement was performed to investigate effect attenuation among retired workers. We also excluded incident AF events that were preceded by a CHD or heart failure event over the follow‐up. Two post hoc analyses were also conducted. First, previous evidence suggests that anger, hostility, and cynicism could be associated with CVD.35 The potential confounding effect of these factors was investigated using validated scales.36 Second, an alternative definition of combined exposure was used, to enhance contrast between groups. In this analysis, participants in passive and active jobs as well as those exposed to low reward without being exposed to an ERI were considered separately. SAS 9.4 software (SAS Institute, Cary, NC) was used for all analyses.
RESULTS
A total of 5926 participants were included in the analyses (2905 men and 3021 women). Participants’ mean age was 45.3 years (±6.7) at baseline and 63.5 years (±6.6) at the end of follow‐up. Over the study period, there were 186 incident AF cases (Table 1), resulting in an incidence rate of 1.71 per 1000 person‐years (95% CI, 1.70–1.71). About half of participants had a university education (47%). There were 34% of participants with sedentary behaviors, and 17% were current smokers. Average body mass index was 25.5 kg/m2, 14% had hypertension (6% on medication), 2% reported having a diagnosis for diabetes, and 27% had hypercholesterolemia. The prevalence of exposure was 19% for job strain and 25% for ERI. Regarding combined exposure, 24% were exposed to either job strain and ERI, while 10% had double exposure. Among 186 participants with incident AF events, 63 (34%) had been diagnosed with CHD or heart failure before AF occurrence.
| Sex | |
| Men | 2905 (49.0) |
| Women | 3021 (51.0) |
| Age, y | 45.3±6.7 |
| Age at the end of follow‐up | 63.5±6.4 |
| Follow‐up duration, y | 18.4±2.4 |
| Atrial fibrillation incident events | 186 (3.1) |
| Prior diagnosis for CHD or heart failure | 63 (33.9)* |
| Education level completed | |
| Less than college | 1495 (25.2%) |
| College | 1640 (27.7%) |
| University | 2791 (47.1%) |
| Income, CAN$ | |
| <30 000 | 443 (7.5%) |
| 30 000–49 999 | 1056 (17.9) |
| 50 000–69 999 | 1712 (29.1) |
| ≥70 000 | 2675 (45.5) |
| Alcohol consumption | |
| Low | 1821 (30.7) |
| Moderate | 3733 (63.0) |
| High | 372 (6.3) |
| Physical activity | |
| ≥3 per wk | 1646 (27.8) |
| 1–2 per wk | 2239 (37.8) |
| <1 per wk (sedentary) | 2041 (34.4) |
| Smoking | |
| Never smoker | 2709 (45.7) |
| Former smoker | 2194 (37.0) |
| Current smoker | 1023 (17.3) |
| Body mass index, kg/m2 | 25.52±4.2 |
| Hypertension | 803 (13.6) |
| Hypertension medication | 335 (5.7) |
| Diabetes | 137 (2.3) |
| Hypercholesterolemia | 1589 (26.8) |
| Family history of CVDs | 2223 (37.5) |
| Job strain | |
| Low job strain | 1044 (17.6) |
| Passive jobs | 2122 (35.8) |
| Active jobs | 1661 (28.0) |
| High job strain | 1099 (18.6) |
| ERI | 1492 (25.2) |
| Combined exposure to high job strain and ERI | |
| Unexposed | 3927 (66.3%) |
| Intermediary: exposed to job strain or ERI | 1407 (23.7%) |
| Double exposure: exposed to job strain and ERI | 592 (10.0%) |
Data are shown as n (%) unless otherwise stated. AF indicates atrial fibrillation; CHD, coronary heart disease; CVD, cardiovascular disease; and ERI, effort–reward imbalance.
*
Among participants with an AF event.
Table 2 presents the association between psychosocial stressors at work and AF incidence. Job strain was associated with an 83% AF risk increase (HR, 1.83 [95% CI, 1.14–2.92]). The association between passive (HR, 1.12 [95% CI, 0.73–1.73]) and active jobs (HR, 1.17 [95% CI, 0.76–1.82]) and AF incidence was not statistically significant. Participants exposed to an ERI had a 44% AF risk increase when compared with unexposed participants (HR, 1.44 [95% CI, 1.05–1.98]). Participants with combined exposure to high job strain and ERI had a 97% AF risk increase (HR, 1.97 [95% CI, 1.26–3.07]). These associations were robust to adjustment for sociodemographic characteristics, lifestyle‐related risk factors, and clinical risk factors.
| Nparticipants=5926; Nevents=186; 108 952 person‐years | Nexposed | Ncase | Crude HR (95% CI)* | HR (95% CI)† | HR (95% CI)‡ | HR (95% CI)§ |
|---|---|---|---|---|---|---|
| Job strain | ||||||
| Low job strain | 1044 | 34 | Reference, 1.00 | |||
| Passive jobs | 2122 | 60 | 0.95 (0.62–1.45) | 1.09 (0.71–1.67) | 1.09 (0.71–1.68) | 1.12 (0.73–1.73) |
| Active jobs | 1661 | 52 | 1.11 (0.72–1.71) | 1.13 (0.73–1.75) | 1.12 (0.73–1.73) | 1.17 (0.76–1.82) |
| High job strain | 1099 | 40 | 1.45 (0.91–2.29) | 1.70 (1.07–2.70) | 1.70 (1.07–2.70) | 1.83 (1.14–2.92) |
| ERI | ||||||
| Unexposed | 4434 | 129 | Reference, 1.00 | |||
| Imbalance state | 1492 | 57 | 1.42 (1.04–1.94) | 1.46 (1.06–1.99) | 1.46 (1.06–2.00) | 1.44 (1.05–1.98) |
| Combined exposure to job strain and ERI | ||||||
| Unexposed | 3927 | 113 | Reference, 1.00 | |||
| Intermediate exposure: high job strain or ERI | 1407 | 49 | 1.31 (0.94–1.84) | 1.34 (0.96–1.88) | 1.36 (0.97–1.90) | 1.34 (0.95–1.88) |
| Double exposure: high job strain and ERI | 592 | 24 | 1.71 (1.10–2.66) | 1.89 (1.21–2.95) | 1.87 (1.20–2.91) | 1.97 (1.26–3.07) |
ERI indicates effort–reward imbalance; and HR, hazard ratio.
*
Crude marginal HR adjusted for age by defining it as time scale and with delayed entry at age of beginning of the study.
†
Additionally adjusted for sex and education.
‡
Additionally adjusted for alcohol consumption, smoking, and physical activity.
§
Additionally adjusted for hypertension, diabetes, hypercholesterolemia, family history of cardiovascular disease, body mass index, and hypertensive medication.
The cumulative incidence of AF was slightly higher among workers exposed to either job strain or ERI at work and aged <60 years (Figure 2). The cumulative incidence associated with combined exposure to both work stressors increased more steeply in comparison, to reach similar progression after the age of 60 years. Interaction terms with sex were not statistically significant for all exposures (Table S1).
Figure 2. Cumulative incidence of atrial fibrillation according to job strain and effort–reward imbalance at work.
AF indicates atrial fibrillation.
Sensitivity analyses are presented in the appendix. Exclusion of AF events occurring within the first 5 years of exposure measurement (N=15) led to similar results, but estimates for job strain were slightly reduced (Table S2). Associations were strengthened in analysis censoring participants at retirement (Table S3). Associations were generally further from the null value in analysis excluding participants with a CHD or heart failure event preceding an AF event (Table S4). Further adjustment for anger, hostility, and cynicism yielded similar estimates (Table S5). Furthermore, the use of the alternative definition for combined exposure led to similar conclusions (Table S6).
DISCUSSION
The aim of the present study was to examine the effect of psychosocial stressors at work from the job strain and ERI models on AF incidence in an 18‐year prospective study. Psychosocial stressors at work from both models were associated with the AF risk, separately and in combination. Associations were robust to adjustment for sex, education, alcohol consumption, smoking, physical activity, body mass index, family history of CVD, diabetes, hypertension, and hypercholesterolemia.
In the present study, workers exposed to job strain had a higher risk of AF (HR, 1.83). Three prospective studies conducted in Sweden had previously examined this association and were summarized in a meta‐analysis (pooled HR, 1.37).14, 15, 16 Methodological considerations including a lower participation at baseline (≤65%),16 alternative job strain assessment based on job titles14 and the use of a shorter follow‐up period16 may partly explain this slightly lower risk estimate. The present study examined the adverse effect of ERI on AF for the first time. Our results showed that workers exposed to an ERI at work had a 44% AF risk increase when compared with unexposed workers. These findings suggest that psychosocial stressors at work from both models should be considered to fully capture the adverse effect of workplace stressors on AF.
In the present study, combined exposure to job strain and ERI was associated with AF risk. Our results are coherent with previous studies, suggesting a deleterious effect of combined exposure on CHD risk.37 In a previous study conducted by our research team, men exposed to both psychosocial stressors at work had more than double the risk of incident CHD compared with those unexposed. A study conducted among Danish workers reported that combined exposure to job strain and ERI was associated with higher CHD risk among men (15%) and women (11%).38 A previous multicohort study reported increased CHD risk ranging from 16% for either exposure to 41% for exposure to both work stressors.8 In the present study, the point estimate of AF risk increase associated with combined exposure was higher than that observed for job strain or ERI considered separately. However, given overlaps in CIs, this finding should be confirmed in future studies.
Excluding AF cases occurring in the first 5 years of follow‐up yielded similar results. Indeed, estimates were slightly attenuated for job strain and combined exposure. This is consistent with results from a previous study on job strain and AF, which have reported similar associations before and after excluding any AF events occurring within the first 5 years.14 However, estimates remained the same for ERI. Of the 186 AF cases observed over the follow‐up, 51 occurred before retirement. In sensitivity analyses censoring at retirement, the association between psychosocial stressors at work and AF incidence was also observed, with slightly higher point estimates. This suggests that the effect could be of higher magnitude when restricting to the period in which participants are still in the workforce. However, results must be interpreted with caution given reduced statistical power and wider CIs. Importantly, our sensitivity analyses also showed that the effect of psychosocial stressors at work on AF is not explained by the precipitating effect of other CVDs, including CHD and heart failure. Primary prevention in workplaces aiming to reduce psychosocial stressors at work may therefore contribute to prevent AF cases among workers without preexisting CVD.
The precise mechanisms by which psychosocial stressors at work increase AF risk are not well understood. However, some pathophysiological mechanisms may directly or indirectly predispose or trigger AF. Exposure to psychosocial stressors is known to activate the autonomic nervous system as well as the hypothalamic–pituitary–adrenal axis and the renin–angiotensin–aldosterone system.39, 40, 41 Exposure to psychosocial stressors at work has been shown to predispose to the development of common clinical conditions associated with AF: hypertension, diabetes, and arterial stiffness.42, 43, 44 Furthermore, the autonomic nervous system may play a more direct role in the initiation and maintenance of AF since surges of both sympathetic and parasympathetic activity have been associated with the onset of AF.45, 46
The present study has limitations. First, job strain and ERI were assessed only once, leading to potential misclassification of exposure over time. This misclassification would likely result in an underestimation of the true association between psychosocial stressors at work and AF risk.47, 48 Second, individuals with missing data on exposure or covariates were excluded. However, a post hoc analysis showed that these excluded participants had similar AF incidence rate when compared with included participants (P=0.56). Selection bias is therefore unlikely. Third, the sensitivity of the algorithm used to identify AF events in medico‐administrative databases was 70.8%, according to a previous validation study using medical records as the gold standard.29 Therefore, a proportion of AF events found in medical records could have been missed. It is reasonable to assume that this potential misclassification is nondifferential regarding the exposure, which could have led to an underestimation of the true effect. Finally, the study population was composed of white‐collar workers. Therefore, generalization may be limited to workers sharing similar occupations. A majority of workers in Canada hold white‐collar occupations,49 favoring generalization to a large segment of the workforce. The adverse effect of psychosocial stressors at work on AF risk among blue‐collar workers should be examined in future studies. Previous evidence suggests that blue‐collar workers have a higher prevalence of exposure to job strain and that the adverse effect of job strain on cardiovascular outcomes is of higher magnitude in this particular population.50, 51
This study also has important strengths. This is the first study to examine the adverse effect of psychosocial stressors at work from both job strain and ERI models on AF risk, in a prospective cohort of men and women followed for 18 years. Participation was high, minimizing the possibility for selection bias. Validated instruments were used for job strain and ERI assessment. Prevalent cases of CVDs were excluded, and the potential effect of main cardiovascular risk factors was accounted for.52, 53
CONCLUSIONS
In the present study, job strain and effort reward imbalance at work were associated with an increased risk of AF incidence over 18 years. Our findings also suggest that work‐stress–related AF could manifest without preexisting CVD events. Prevention strategies targeting psychosocial stressors at work could provide benefits to reduce the public health and economic burden associated with AF. A workplace intervention aiming to reduce job strain and ERI exposures was shown to be effective to reduce BP means and hypertension prevalence among workers.54 Therefore, such interventions may be effective to reduce the burden associated with AF at the population level.
Sources of Funding
This work was supported by Canadian Institutes for Health Research (MA‐11364).
Disclosures
None.
Acknowledgments
This work was performed at the Centre Hospitalier Universitaire (Hospital Research Center) de Québec‐Université Laval Research, Québec City, Canada. All the authors contributed to this work.
Footnotes
This manuscript was sent to Tiffany M. Powell‐Wiley, MD MPH, Associate Editor, for review by expert referees, editorial decision, and final disposition.
Supplemental Material is available at Supplemental Material
For Sources of Funding and Disclosures, see page 8.
Supplemental Material
Data S1
Tables S1–S6
Figure S1
Reference 55
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© 2024 The Author(s). Published on behalf of the American Heart Association, Inc., by Wiley. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
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Received: 31 August 2023
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Canadian Institutes for Health Research: MA‐11364
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